The role played by the renin-angiotensin axis in the causation of preglomerular vasoconstriction and decreased renal blood flow in ischemic and toxic renal damage will be studied. Rats with tenin depleted kidneys will be produced by salt overload. In another group, renin synthesis will be increased by dehydration, salt deficient diet, and ethacrynic acid administration. Decreased angiotensin converting enzyme inhibitor and specific inhibitor of angiotensin II. Ischemic renal injury and acute tubular necrosis will be produced in the three groups by total temporary ischemic, hemorrhagic hypotension, and mercuric chloride. A comparative study of the renal vasculature of injured kidneys in the three groups will be undertaken by the techniques of in vivo carbon perfusion, angiography, and silicone rubber casting, freeze substitution and electron microscopy. It is expected that renin depletion and decreased angiotensin activity will inhibit preglomerular vasoconstriction and enhance renal blood flow, whereas increased synthesis of renal renin will lead to excessive vasoconstriction and decreased blood flow. If the expected differences are found experimentally, they will demonstrate the relationship between the renin angiotensin axis, preglomerular vasoconstriction, and decreased renal blood flow. The results will then contribute to a better understanding of deranged renal function in acute tubular necrosis.